Exposure to stress can disrupt the secretion of luteinizing hormone (LH) and subsequent ovulation. One avenue by which stress can disrupt ovulation is by altering the hypothalamic control of gonadotropin release. One of the key mediators of the brain's stress response is norepinephrine (NE), and hypothalamic/preoptic area NE plays a pivotal role in the coordination of female reproduction by gonadal steroids. Possibly, stress blocks ovulation by altering the pattern of NE neurotransmission in the hypothalamus/preoptic area. This proposal will test the hypothesis that stress disrupts the proestrous LH surge by hyperstimulating NE release to levels that are inhibitory to gonadotropin-releasing hormone (GnRH) neurons. Specific Aim I will use c-fos immunocytochemistry to examine if stress alters the normal activation of GnRH neurons on proestrus. Specific Aim 2 will use in vivo microdialysis to examine if stress increases NE neurotransmission in brain regions important for GnRH secretion. Specific Aim 3 will use microinfusions of NE into specific brain regions to test if supranormal NE levels block the proestrous LH surge. Specific Aim 4 will examine whether supranormal NE blocks the proestrous LH surge by stimulating another neurotransmitter system, corticotropin releasing factor.